Image data related to publication "Size-dependent plastic exposure disrupts macrophage function and tissue-specific metabolism"doi:10.60507/FK2/M42B8Obonndata2026-01-211Makdissi, Nikola; Viola, Maria Francesca; Mass, Elvira, 2026, "Image data related to publication "Size-dependent plastic exposure disrupts macrophage function and tissue-specific metabolism"", https://doi.org/10.60507/FK2/M42B8O, bonndata, V1Image data related to publication "Size-dependent plastic exposure disrupts macrophage function and tissue-specific metabolism"doi:10.60507/FK2/M42B8OMakdissi, NikolaViola, Maria FrancescaMass, ElviraDagmar WachtenVirginia AliprandiMarina MayerKatharina SieckmannNele Kronau851257ATLF 873-2023GRK1873/2bonndataMass, ElviraMakdissi, Nikola2025-12-20Medicine, Health and Life SciencesMedicine, Health and Life SciencesPlastic pollution is an emerging yet understudied environmental risk to the immune system. Once ingested, nano- and microplastic particles (MNPs) can translocate from the gut to internal organs, with macrophages serving as primary targets. Kupffer cells (KCs), the liver-resident macrophages, play a central role in immune surveillance and metabolism, yet their response to MNPs remains unclear. Here, using a chronic plastic exposure model in mice, we identify KCs as the primary hepatic reservoir for MNPs. Long-term exposure alters their transcriptional profile and impairs phagocytic function, leading to metabolic dysregulation of hepatocytes. Microplastics, but not nanoplastics, reduce KC-mediated clearance of circulating cells and bacteria. Under diet-induced obesity, microplastics exacerbates hepatic lipid accumulation, while nanoplastics impair systemic glucose metabolism. Although the blood-brain barrier limits microplastic infiltration, a small fraction of ingested nanoplastics reaches the brain, where it is taken up by microglia, the brain-resident macrophages. However, we observe no signs of neuroinflammation or behavioral deficits. These findings demonstrate that chronic MNP exposure disrupts macrophage function in a size-dependent manner, with distinct consequences for liver and systemic metabolism, while the brain remains largely protected. Understanding tissue-specific vulnerabilities to MNPs is crucial for assessing their long-term health impact.<a href="http://creativecommons.org/licenses/by/4.0">CC BY 4.0</a>Nikola Makdissi, Maria Francesca Viola, Lisa Steinheuer et al. Size-dependent plastic exposure disrupts macrophage function and tissue-specific metabolism, PREPRINT (Version 1) available at Research Square10.21203/rs.3.rs-6204281/v1Nikola Makdissi, Maria Francesca Viola, Lisa Steinheuer et al. Size-dependent plastic exposure disrupts macrophage function and tissue-specific metabolism, PREPRINT (Version 1) available at Research SquareGFAP_MP.zipapplication/zipGFAP_NP.zipapplication/zipGFAP_PBS.zipapplication/zipgWAT_HE_NMPingestion.zipapplication/zipIF_NMPingestion_Clec4f-DTR.zipapplication/zipInsulinIHC_NMP_HFDingestion.zipapplication/zipORO_NMPingestion.zipapplication/zipPAS_NMPingestion.zipapplication/zipReadme_Makdissi_Viola_ ImageData_PlasticExposure.txttext/plain